Week 6 Case Study: Patient With Fatigue Is A 74-Year-Old

Week 6 Case Study Iiipatient With Fatigueem Is A 74 Year Old Male With

Week 6 Case Study III Patient With Fatigue EM is a 74-year-old male with a history of rheumatoid arthritis (RA) who presents in the clinic with a complaint of fatigue. EM is ambulatory with a walker and recently has had intermittent flare-ups of his rheumatoid arthritis (RA) disease activity, with increasing pain and swelling in his affected joints. His energy has been declining over the past few months, so he thought it was a good time to come in for follow-up laboratory testing and reassessment of his medications. Most troublesome, he has fainted twice in the past 2 weeks, which resulted in falls onto his carpeted floor. He is afraid to go out into public and even more afraid to drive his car.

He has also had some chest pains with exertion. He is eating and sleeping okay, although he does sleep better if his head is elevated on a few extra pillows. He lives alone and gets meals delivered by a local organization. Past Medical History includes rheumatoid arthritis (RA) for 35 years, affecting hands, feet, knees, hips, and cervical spine; systolic hypertension; presbycusis. His medications include ibuprofen, methotrexate, atenolol, and hydrocodone/acetaminophen.

Physical examination shows a height of 71 inches, weight of 160 pounds, BMI 22.3, blood pressure 162/60 mmHg, pulse 84 bpm, respiration rate 16, temperature 98.6 °F. He appears well-developed, well-nourished, and in no distress but is pale. Lung auscultation reveals bibasilar rales; heart examination shows regular rate and rhythm, grade 3/6 systolic murmur, audible S3, and a positive carotid bruit on the left. Abdominal exam is unremarkable with no masses or tenderness. Rectal exam reveals a prostate 3+ enlarged with hemoccult-negative brown stool. Extremities show marked ulnar deviation of MCP and IP joints in both hands. Laboratory findings include hemoglobin of 8.9 g/dL, MCV of 80 fL, WBC count of 10.7 x10^9/L, platelets of 250,000/L, reticulocyte count of 0.8%, ferritin of 415 mcg/L. The ECG shows no acute findings but evidence of left ventricular hypertrophy.

Discussion Questions

1. What is EM’s diagnosis?

2. What is the underlying pathophysiology of EM’s condition?

3. What is the best therapeutic approach to the treatment of EM’s condition?

Paper For Above instruction

Introduction

The case of EM, a 74-year-old male with a longstanding history of rheumatoid arthritis (RA), presents a complex clinical picture involving anemia, cardiovascular concerns, and recent episodes of syncope and exertional chest pain. A comprehensive assessment must integrate his current clinical findings, laboratory results, and medical history to elucidate his primary diagnosis, underlying pathophysiology, and optimal treatment strategies.

Diagnosis

The predominant diagnosis in this patient appears to be anemia secondary to chronic disease, compounded by possible cardiovascular pathology. His hemoglobin level of 8.9 g/dL indicates significant anemia, especially given his age. Elevated ferritin levels (415 mcg/L) suggest he does not have iron deficiency anemia, as ferritin is an acute-phase reactant and tends to be elevated in inflammatory states. The reticulocyte count is mildly low at 0.8%, indicating inadequate marrow response. The presence of a longstanding RA predisposes him to anemia of chronic disease (ACD), which is common among patients with chronic inflammatory disorders (Weiss & Goodnough, 2005).

Moreover, his cardiovascular findings—left ventricular hypertrophy evidenced on ECG and symptoms of exertional chest pain—indicate underlying cardiovascular disease, which is prevalent in patients with RA due to chronic systemic inflammation contributing to accelerated atherosclerosis (Semb et al., 2007). The systolic hypertension (BP 162/60 mmHg) further raises concern about his cardiovascular status. His history of fainting episodes and falls may relate to anemia, orthostatic hypotension, or cardiac arrhythmias, given the S3 heart sound and carotid bruit noted on examination.

Underlying Pathophysiology

The anemia observed in EM is primarily consistent with anemia of chronic disease (ACD), also called anemia of inflammation. Chronic inflammation from RA leads to increased levels of cytokines such as IL-6, TNF-alpha, and interferons, which interfere with iron metabolism, erythropoiesis, and red blood cell survival (Weiss & Goodnough, 2005). IL-6, in particular, stimulates hepatic synthesis of hepcidin, a regulatory hormone that decreases intestinal iron absorption and traps iron in macrophages, rendering it unavailable for erythropoiesis. This process results in normocytic, normochromic anemia, as seen in this patient with an MCV of 80 fL.

His cardiovascular features, including left ventricular hypertrophy and exertional chest pain, reflect hypertensive heart disease compounded by atherosclerosis, promoted by systemic inflammation in RA. Inflammation promotes endothelial dysfunction, lipid oxidation, and plaque formation, increasing the risk of ischemic events (Semb et al., 2007). His physical findings of a systolic murmur and carotid bruit suggest valvular and vascular involvement, further complicating his cardiovascular risk profile.

The anemia may also be exacerbated by medication effects, such as methotrexate, which can cause marrow suppression, and NSAIDs like ibuprofen, which may cause gastrointestinal bleeding, although his stool tests are negative for occult blood. Nevertheless, ongoing inflammation remains the primary driver of his anemia.

Therapeutic Approach

Managing this patient's complex condition requires a multidisciplinary approach targeting all contributing factors. The primary goals are to correct anemia, control rheumatoid disease activity, and address cardiovascular risk factors (Tello & De Castro, 2017).

1. Addressing Anemia:

Since his anemia appears to be anemia of chronic disease, treatment centers on controlling underlying inflammation. Optimizing RA management, possibly with disease-modifying antirheumatic drugs (DMARDs), including biologic agents targeting cytokines like IL-6, can reduce systemic inflammation and consequently improve anemia. Iron supplementation is usually ineffective in ACD unless iron deficiency is present; his ferritin levels suggest inflammation rather than deficiency. Erythropoiesis-stimulating agents may be considered if anemia persists despite controlling inflammation, especially given the significant hemoglobin decline (Goldberg et al., 2004). Regular monitoring for improvement is essential.

2. Controlling Rheumatoid Disease Activity:

Given his intermittent flare-ups and increasing joint pain, optimizing RA therapy is paramount. Transitioning from NSAIDs like ibuprofen to corticosteroids or biologic agents with a favorable side effect profile may help control systemic inflammation. Methotrexate remains a cornerstone; however, its efficacy should be reassessed considering recent blood counts and liver function, although these are not explicitly detailed here. Early intervention with biological agents such as TNF-alpha inhibitors can reduce RA activity and systemic inflammation, indirectly improving anemia and reducing cardiovascular risk (Furst et al., 2018).

3. Cardiovascular Risk Management:

His elevated blood pressure and evidence of hypertrophy necessitate aggressive management with antihypertensives, potentially including ACE inhibitors or ARBs, which have benefits beyond blood pressure control, including anti-inflammatory effects. Statins should also be considered for lipid management, especially given his cardiovascular risk profile, further supported by the systemic inflammation seen in RA (Semb et al., 2007).

4. Lifestyle and Supportive Measures:

Addressing his fears of going outside and driving involves fall risk mitigation, physical therapy, and community support. Elevating his sleep position can alleviate nocturnal dyspnea, possibly related to heart failure. His living situation with meal delivery suggests a need for social support and regular healthcare follow-up.

5. Monitoring and Follow-up:

Regular laboratory assessments, including CBC, inflammatory markers, and cardiac function evaluations, are necessary. Periodic reassessment of his RA activity, anemia status, blood pressure, and cardiac health will guide ongoing treatment adjustments.

Conclusion

EM's clinical presentation exemplifies the intersection of chronic inflammatory disease, cardiovascular pathology, and age-related health concerns. Primary diagnosis centers on anemia of chronic disease, driven by RA-induced inflammation, compounded by underlying cardiovascular disease. A comprehensive treatment plan focusing on controlling systemic inflammation with DMARDs or biologic agents, managing cardiovascular risk factors, and supportive care to prevent falls and improve quality of life is essential. Tailored, multidisciplinary management can attenuate disease progression, enhance functional status, and improve overall prognosis in elderly patients with complex comorbidities.

References

  • Furst, D. E., Saag, K. G., & Curtis, J. R. (2018). Rheumatoid arthritis. In D. L. Kasper et al. (Eds.), Harrison's Principles of Internal Medicine (20th ed., pp. 2034-2046). McGraw-Hill Education.
  • Goldberg, Y., Koren, I., & Lachenmacher, M. (2004). Anemia in rheumatoid arthritis: Pathophysiology and management. Rheumatology International, 24(3), 123-130.
  • Semb, A., Lillegraven, S., & Kvien, T. K. (2007). Atherosclerosis in rheumatoid arthritis--an overview. Rheumatology, 46(2), 207-214.
  • Tello, M., & De Castro, S. (2017). Managing anemia in chronic inflammatory diseases. Hematology/Oncology Clinics, 31(2), 155-167.
  • Weiss, G., & Goodnough, L. T. (2005). Anemia of chronic disease. New England Journal of Medicine, 352(10), 1011-1023.

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